Role of mammalian cytosolic molybdenum Fe–S flavin hydroxylases in hepatic injury

Abstract The study was designed to investigate the role of molybdenum iron–sulfur flavin hydroxylases in the pathogenesis of liver injuries induced by structurally and mechanistically diverse hepatotoxicants. While carbon tetrachloride (CCl 4 ), thioacetamide (TAA) and chloroform (CHCl 3 ) inflict liver damage by producing free radicals, acetaminophen (AAP) and bromobenzene (BB) exert their effects by severe glutathione depletion. Appropriate doses of these compounds were administered to induce liver injury in rats. The activities of the Mo–Fe–S flavin hydroxylases were measured and correlated with the biochemical markers of hepatic injury. The activity levels of the anti-oxidative enzymes and glutathione redox cycling enzymes were also determined. The treatment of rats with the hepatotoxins that inflict liver injury by generating free radicals (CCl 4 , TAA, CHCl 3 ) had elevated activity levels of hepatic Mo–Fe–S flavin hydroxylases ( p